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Open AccessJournal ArticleDOI

Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.

TLDR
It is shown that gammadelta T cells express IL-23R and the transcription factor RORgammat and produce IL-17, IL-21, and IL-22 in response to IL-1beta andIL-23, without T cell receptor engagement.
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This article is published in Immunity.The article was published on 2009-08-21 and is currently open access. It has received 1410 citations till now. The article focuses on the topics: T cell & Interleukin 17.

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Citations
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Journal ArticleDOI

Intestinal homeostasis and its breakdown in inflammatory bowel disease

TL;DR: It is now evident that immune effector modules that drive intestinal inflammation are conserved across innate and adaptive leukocytes and can be controlled by host regulatory cells.
Journal ArticleDOI

Regulation and Functions of the IL-10 Family of Cytokines in Inflammation and Disease

TL;DR: The IL-10 family of cytokines consists of nine members that can promote innate immune responses from tissue epithelia to limit the damage caused by viral and bacterial infections and facilitate the tissue-healing process in injuries caused by infection or inflammation.
Journal ArticleDOI

The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

TL;DR: Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge, and a review presents and integrates recent progress in the field.
Journal ArticleDOI

Innate IL-17-producing cells: the sentinels of the immune system

TL;DR: The many innate immune cell populations that are an early source of IL-17 in response to stress, injury or pathogens are explored.
References
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Journal ArticleDOI

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.

TL;DR: It is shown that IL-6, an acute phase protein induced during inflammation, completely inhibits the generation of Foxp3+ Treg cells induced by TGF-β, and the data demonstrate a dichotomy in thegeneration of pathogenic (TH17) T cells that induce autoimmunity and regulatory (Foxp3+) T Cells that inhibit autoimmune tissue injury.
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The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells.

TL;DR: It is shown that the orphan nuclear receptor RORgammat is the key transcription factor that orchestrates the differentiation of this effector cell lineage of proinflammatory T helper cells and its potential as a therapeutic target in inflammatory diseases is highlighted.
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Interleukin 17–producing CD4 + effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

TL;DR: Findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.
Journal ArticleDOI

A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

TL;DR: In vivo, antibody to IL- 17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused Chemokine production and leukocyte infiltration, indicating a unique T helper lineage that regulates tissue inflammation.
Journal ArticleDOI

IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

TL;DR: Using passive transfer studies, it is confirmed that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.
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